POS0491 EVALUATION OF FRACTURE PREVALENCE AND RISK IN A MONOCENTRIC COHORT OF PATIENTS WITH NON-METASTATIC BREAST CANCER IN ADJUVANT ENDOCRINE THERAPY TREATED WITH ANTIRESORPTIVE DRUGS
Authors: M. Pontalti, M. Felicetti, M. A. Jaber, R. Bortolotti
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Bone loss is one of the major long-term side effects of adjuvant endocrine therapy for breast cancer. There is limited consensus on how to accurately assess fracture risk in this setting. Many trials showed the effectiveness of antiresorptive drugs in preventing the loss of bone mineral density (BMD) and, consequently, reducing fracture risk [1]. <h3>Objectives</h3> Our study aims to investigate osteoporotic fractures prevalence and to assess the age adjusted fractures risk in breast cancer patients receiving AET and treated with antiresorptive drugs. Moreover, we analyzed differences in terms of clinical features and outcomes between patients treated with denosumab (DMAB) or bisphosphonates (BPs), and examined variations in biochemical markers of bone turnover and densitometric values to assess the effects of each antiresorptive medication. <h3>Methods</h3> In this monocentric, retrospective, non-randomized cohort study we enrolled patients with non-metastatic breast cancer who received at least 5 years of AET and were treated with DMABs or BPs. We retrieved demographic and clinical data pertaining to the cancer characteristics and the osteoporotic risk at the start of the antiresorptive therapy (baseline), as well as serum levels of C-terminal telopeptide of type I collagen (CTX), vitamin D, parathyroid hormone (PTH), and densitometric data (DXA) at baseline and at 24 months. <h3>Results</h3> We enrolled 120 patients, 38 on DMABs and 82 on BPs. During a median follow-up of 32 months (24-38), 16 (13.3%) fractured at least once. At baseline, the latter had lower BMI [22 kg/m<sup>2</sup> (21-27) vs 24 kg/m<sup>2</sup> (20-26), p=0.043], higher prevalence of osteoporosis (12/16 vs 35/104, p=0.002), higher prevalence of prior fractures (8/16 vs 15/104, p=0.003), and lower AET exposure time [2.7 years (1.2-3.7) vs 3.8 years (2.4-5.8), p=0.008]. In age-adjusted Cox-proportional model, a history of previous fractures and BMD at the femoral neck &lt;-2 at baseline were associated with higher fracture risk [HR 7.8 (2.7-22.9), p&lt;0.001, and HR 3.4 (1.1-10.4), p=0.033, respectively], whereas higher levels of vitamin D resulted protective [HR 0.7 (0.5-0.9), p=0.010]. AET exposure time and the type of antiresorptive drug, instead, had no impact on the fracture risk. Patients who received DMAB had significantly lower levels of vitamin D, age and AET exposure time [33 ng/ml (26-39) vs 36 ng/ml (30-41), p=0.022, 55 years (10.2) vs 60 years (9.1), p=0.008, and 2.9 years (2.0-4.4) vs 3.9 years (2.6-5.9), p=0.014, correspondingly]. At 24 months, both medications were successful in reducing serum levels of bone resorption markers and increasing densitometric values. The DMAB group experienced substantially larger BMD increases in the lumbar spine and femoral neck [respectively, +9.0% (+4.2/+19.8) vs +3.3% (-1.3/+6.6), p&lt;0.001, and +6.1% (+2.2/+15.5) vs +0.7% (-3.5/+4.4), p&lt;0.001]. <h3>Conclusion</h3> The frequency of fractures tends to stay high in women receiving AET even if on antiresorptive drugs despite biochemical and instrumental improvements, indicating the existence of other concurrent processes of bone damage. To enable quick management of bone health-related issues, a thorough risk assessment must be done at the moment AET is started. When given based on risk stratification, DMABs and BPs seem to have comparable antifracture effectiveness profiles. DMAB, however, was more successful in increasing BMD over time. Whatever the case, we found that appropriate vitamin D supplementation is advised throughout AET. <h3>References</h3> [1]Gnant M, Pfeiler G, Dubsky PC, Hubalek M, Greil R, Jakesz R, et al. Adjuvant denosumab in breast cancer (ABCSG-18): a multicentre, randomised, double- blind, placebo-controlled trial. Lancet. 2015 Aug 1; 386(9992):433–43 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.